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[See:  Hemiptera Key]


          This is a disease caused by Trypanosoma cruzi in some non-urban areas of subtropical and tropical America.  The disease is vectored by various species of insects in the hemipteran family Reduviidae.  Frequently in rural areas dwellings may be heavily infested with the true bugs of this family that draw blood from the human occupants all through the night.  Service (2008) reports that blood loss from these insects can exceed 2 ml per person every night, which if prolonged can result in anemia.




       In the Hemimetabolous life cycle the eggs hatch after 10-15 days incubation to produce small nymphs that resemble adults and which go through about five stages of development.  Like the adults, the nymphs feed on blood, doing so mainly at night.  They tend to seek out a host's  head area for their blood meals.  People are not normally aware that feeding has occurred because there is little sensation.  Detection of their presence is by observing cast molting skins and streaks of fecal material in the houses.  The life cycle is quite long: about 3-10 months or sometimes even 1-2 years (Service 2008).  All stages are able to survive for several months without a blood meal.  A large array of wild animals, including squirrels mice, lizards and cattle, are attacked and may serve as reservoir hosts.


       The vectors ingest the parasite's trypomastigotes that reside in a host during a blood meal.  The parasites then continue their development within the insect's intestines.  There they further develop into epimastigotes and multiply to great numbers.  Within 8 to 17 days these develop into infective metacyclic trypomastigotes in the lumen of the insect's posterior intestines.   Vectors will regularly feed for 10-25 minutes or longer, during which time many species of bugs excrete liquid or semi liquid feces that may be contaminated with the metacyclic form of Trypanosoma cruzi that were derived from an earlier blood meal.  Infection in humans occurs when bug excreta are scratched either into skin abrasions or through the wound of the bug's bite, or when it might be rubbed into the eyes or other mucous membranes.  Transmission results then only through the insect's feces and not directly by its bite.


       Service (2008) reported that there are some 70 species of Reduviidae that have been found infected with T. cruzi, but only about 12 species that live in close association with humans and feed on them.  Principal vector species are Triatoma infestans (southern South America), Pangastrongylus megistus (southeastern Brazil), Rhodnius prolixus (Honduras, Nicaragua, Colombia & Venezuela) and Triatoma dimidiata (Mexico through northwestern South America).  The efficiency of a vector depends on how long it feeds on a human and if it defecates during feeding.  However, Trypanosoma rangeli that occurs from Mexico to Brazil and is transmitted by Rhodnius prolixus, can infect humans directly by its bite.


       A further discussion of the disease organism given by Service (2008) explained that Trypanosoma cruzi is really a parasite of wild animals, such as opossums, armadillos and wild and urgan rats mice, squirrels, monkeys, etc. that may serve as reservoir hosts.  Simply eating the vectors or infected animals can infect them.  In some cases humans can also aquire infection by eating infected meat or food that is contaminated with infective bug excrement. The insect itself may also be an infection reservoir, but in some areas humans are thought to be the main reservoir hosts. 


       Infection rates in vector populations can frequently be very high.  Service (2008) reported that it is common to find infection rates of around 25 percent or higher.  In California the Triatoma protracta population can be 78 percent, but it rarely bites humans.  Although vectors can account for more than 80 percent of transmission, blood transfusions account for 17 percent and congenital transmission 2 percent.




       Chagas Disease is generally controlled by insecticide applications to the interior surfaces of dwellings even though resistance to the insecticide develops rapidly.  Fumigation is effective but must be done regularly.  More permanent but expensive control involves altering dwelling structures so as to make them less attractive vector resting sites.  Service (2008) noted that such alterations include plastering walls to cover cracks and replacing thatched dwellings with those constructed with bricks or concrete blocks, and having metal roofs.  Because of the high rates of infection among the human populations of northwestern South America, governments there are launching massive efforts to inform and assist the public in vector control.


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 Key References:     <medvet.ref.htm>    <Hexapoda>


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Brenner, R. R. & A. M. Stoka.  1988.  Chagas Disease Vectors I: Taxonomic, Ecological & Epidemiological Aspects.  CRC Press, Boca

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      Oswaldo Cruz Fundacion.

Kingman, S.  1991.  South America declares war on Chagas disease.  New Scientist (19 Oct) pp. 16-17.

Lent, H. & P. Wygodzinsky.  1979.  Revision of the Triatominae (Hemiptera, Reduviidae), and their significance as vectors of Chagas disease.

        Bull.Amer. Mus. Nat. Hist. 163:  123-520.

Matheson, R. 1950.  Medical Entomology.  Comstock Publ. Co, Inc.  610 p.

Moncayo, A. & M. I. Ortiz-Yanine.  2006.  An update on Chagas disease (human trypanosomiasis).  A.. Trop. Med. & Parasit. 100:  663-77.

Schofield, C. J. & J. P. Dujardin.  1997.  Chagas disease vector control in Central America.  Parasitology Today 13:  141-44.

Service, M.  2008.  Medical Entomology For Students.  Cambridge Univ. Press.  289 p

Legner, E. F.  1995.  Biological control of Diptera of medical and veterinary importance.  J. Vector Ecology 20(1): 59_120.

Legner, E. F.  2000.  Biological control of aquatic Diptera.  p. 847_870.  Contributions to a Manual of Palaearctic Diptera,

          Vol. 1, Science  Herald, Budapest.  978 p.

Yamagata, Y. & J. Nakagawa.  2006.  Control of Chagas disease.  Adv. in Parasitology 61:  129-65.